Effect of heparin-induced elevation of free fatty acids on myocardial oxygen consumption in man

1976 ◽  
Vol 37 (1) ◽  
pp. 167 ◽  
Author(s):  
William J. Rogers ◽  
Richard O. Russell ◽  
Roger E. Moraski ◽  
Huey G. McDaniel ◽  
Charles E. Rackley
Cardiology ◽  
1973 ◽  
Vol 58 (4) ◽  
pp. 220-228 ◽  
Author(s):  
Albert S. Most ◽  
Milton H. Lipsky ◽  
Patricia A. Szydlik ◽  
Carl Bruno

1988 ◽  
Vol 255 (1) ◽  
pp. H169-H176 ◽  
Author(s):  
A. J. Liedtke ◽  
L. DeMaison ◽  
S. H. Nellis

We tested the influence of L-propionylcarnitine (LPC) in modifying mechanical stunning during reflow. Nineteen adolescent anesthetized swine were extracorporeally perfused at control coronary flows for 20 min, supplemented with excess fatty acids (average values 1.1 +/- 0.1 mumol/ml), and subjected to 45 min regional ischemia (-60 delta % decrease in anterior descending flow) followed by 35 min reperfusion. Responses in 10 placebo hearts were compared with those obtained from 9 animals treated with 50 mg/kg LPC at 0 min perfusion and 40 mg/kg at 40 min perfusion. Ischemia in placebo hearts caused a 62.6 delta % decrease in active shortening in anterior descending bed, which failed to recover (-41.4 delta % from control values) during reflow. Conversely, in LPC-treated hearts, decreases in active shortening (-38.6 and -11.6 delta %) during ischemia and reflow, respectively, were significantly smaller (P less than or equal to 0.05). This improved motion was associated with greater rates of myocardial oxygen consumption but similar levels of fatty acid oxidation and fatty acid intermediates. Thus LPC significantly reversed mechanical stunning in myocardial ischemia/reperfusion protocols, presumably because of its positive inotropic properties. This derivative, otherwise innocuous in nature, could represent an attractive new treatment choice for future clinical use.


1979 ◽  
Vol 57 (7) ◽  
pp. 725-730 ◽  
Author(s):  
Louise Lafrance ◽  
Danièle Routhier ◽  
Bernard Têtu ◽  
Christian Têtu

A 3-h noradrenaline (NA) infusion (1.5 μg kg−1 min−1) produced a sustained enhanced oxygen consumption (O2 cons.) in cold-adapted rats. Plama free fatty acid (FFA) levels were elevated by NA in control and in cold-adapted rats, but to a lesser extent in cold-adapted rats; the increase was maintained at a plateau in both groups during the entire period of NA infusion. A 1-h nicotinic acid (Nic A) infusion (1.5 mg kg−1 min−1) added to the NA infusion inhibited the calorigenic response to NA in cold-adapted rats and reduced the elevated plasma FFA concentration in control and in cold-adapted rats to values below basal levels. However, when the Nic A infusion was stopped, the O2 cons, was increased again in cold-adapted rats by the uninterrupted NA infusion, without the simultaneous increase of the plasma FFA concentration; the plasma FFA concentration was maintained in cold-adapted rats below basal values and merely brought back to basal levels in control rats. From these results, it is suggested that plasma FFA are not an essential substrate to the calorigenic response to NA observed in cold-adapted rats, as 85% of the response can occur when the plasma FFA concentration is very low.


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